1 / 45

Emergency treatment of A cute O rganophosphate P esticides P oisoning (A O P P)

Emergency treatment of A cute O rganophosphate P esticides P oisoning (A O P P). Emergency department Wenzhou People’s hospital 吴瑞克. Content. Classification Pathogenesy Manifestation Management. Characteristics. Oily Smell like garlic.

snobles
Download Presentation

Emergency treatment of A cute O rganophosphate P esticides P oisoning (A O P P)

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. Emergency treatment ofAcute Organophosphate Pesticides Poisoning (A O P P) Emergency department Wenzhou People’s hospital 吴瑞克

  2. Content • Classification • Pathogenesy • Manifestation • Management

  3. Characteristics • Oily • Smell like garlic. • It can easily be decomposed under alkaline conditions.

  4. Characteristics • ThepatientswithAOPParesometimesincriticalcondition. • Afterpropertreatmentsintimemostofthepatient’slivescanberescued.

  5. Classification

  6. 其次：肾、 肺、脾等 浓度最高 • Routes of entry： • Skin • Resp. tract • GI. tract Enterohepatic circulation

  7. Pathogenesy • The primary mechanism of action of OP is inhibition of acetylcholinesterase(AChE): Phosphate+AChE →Phospharylated AChE→ The Acetylcholine(ACh) ↑↑

  8. Pathogenesy • The Ach accumulates throughout the nervous system, resulting in overstimulation of muscarinic and nicotinic recepters which can be found in the nervous system and neuromuscular junction.

  9. Normal Nerve Function Postsynaptic membrane Motor end-plate Presynaptic membrane ACh Synapse Neuromuscular junction

  10. Normal Nerve Function Postsynaptic membrane Motor end-plate Presynaptic membrane ACh M and N receptor Synapse Neuromuscular junction

  11. Normal Nerve Function Hydrolyze acetylcholine AChE ACh Synapse Neuromuscular junction

  12. How OP Works: Reversible & Aged Binding AChE OPs ACh Synapse Neuromuscular junction

  13. CNS effects Nicotinic effects • Muscarinic effects

  14. Manifestations • 1.Cholinergic crisis • Muscarinic effects • Nicotinic effects • CNS effects • 2.Intermediate syndrome(IMS) • 3.Organophosphate-induced delayed polyneuropathy (OPIDP) Signs and symptoms of OPs poisoning can be divided into 3 broad categories.

  15. Muscarinic effects is duo to excessive parasympathetic activation. • Smooth muscle spasm • GI: nausea, vomite, abdominal pain, increased peristaltic sounds. • Urinary tract: frequency of urination, urinary incontinence. • Bronchus: tachypnea, dyspnea. • Ocular: pinpoint pupil(miosis), blurred vision. • Sphincter relaxation • Incontinence of urine and feces • Cardiovascular symptoms • Bradycardia, hypotension • Over active Glands(sympathetic cholinergic nervous ) • Increased lacrimation, diaphoresis • Sputum and moist rale, diarrhea

  16. Nicotinic effects • Stimulation of muscle motor end-plate • Fasciculation → Weakness →Paralysis • Respiratory muscle paralysis →peripheral respiratory failure • Stimulation of sympathetic nervous system • Tachycardia • Hypertension • Arrhythmia

  17. CNS symptom • Serious effects • Coma • Respiratory centre depression(Central RF) • Seizures • Other effects • Confusion • Memory loss • Disorientation • Delirium

  18. Intermediate syndrome(IMS) • Typically 1-3 days after cholinergic crisis has resolved, and before delayed polyneuropathy. • Proximal muscle weakness and cranial nerve lesions. • Delayed Respiratory Failure.

  19. Mechanism of IMS • Prolonged Effects on Nicotinic receptors because of the accumulation of Ach in the neuromuscular junction → Motor end-plate degeneration → Neuromuscular block →Peripheral respiratory failure

  20. Clinical importance of IMS • Delayed respiratory failure leads to death if not aware of it or prepared for it. • Mechanical ventilation may be the only effective emergency measures.

  21. Organophosphate-induced delayed polyneuropathy (OPIDP) • Occurs 1-5 weeks after exposure to large doses of certain OPs. • Begin with shooting pains in both legs, then upper extremities. • Quadriplegia. • Standard treatments are ineffective.

  22. Complications • 1.Respiratory failure • 2.Shock • myocardial injury, cardiac contractility reduced, cardiac arrhythmia. • Peripheral circulatory failure, angiectasis. • Inhibition of the cardiovascular central. • Hypovolemic shock due to dehydration. • 3.Malignant arrhythmia. • 4.Brain edema.

  23. Laboratory Studies • Measurement of acetylcholinesterase (AChE)activity. • Most widely used for a diagnosis of OP, for judgement of severity andeffect of treatment. • It is an objective indicator which can be a guidance for the dosage of antidote.

  24. Management The priority in management is : • Resuscitation!

  25. Resuscitation • Recognition of life threatening events when you work in ED. • The ABCDE approach is the prior task we have to do in early treatment of critical illness.

  26. The ABCDE approach A E B Airway & assessment Exposure & examination D C Breathing , ventilation & oxygenation Disability due to neurological deterioration Circulation & shock management

  27. Gastrointestinal Decontamination • 1. Gastric lavage：Usualy use warm water. Every time 300-500ml,10,000-30,000ml in total，until the liquid washing out is clear and without the smell of OPs.Feed Activated Charcoal via nasal-gastric tubeafter gastric lavage. 2%sodium bicarbonate（dipterex） 1:5000potassium permanganate（parathion, malathion） • 2. Catharsis: 20%Mannitol Na2SO4 The effect maybe not obvious because of a high dose of atropine.

  28. Gastrointestinal Decontamination • GI Decontamination is NOT a life saving procedure! • Should not be performed before resuscitation

  29. Benefits Gastrointestinal Decontamination Risks • Aspiration • Trauma • Electrolyte Imbalances • Cardiac Arrest • Removal of poison load • Prevention of ongoing poison absorption

  30. Medication • Cholinesterase reactivator — Pralidoxime • Anticholinergic drugs — Atropine,Scopolamine

  31. 1、Cholinesterase reactivator • Pralidoxime——release nicotinic effect. • Giving the pralidoxime sufficiently and in time can improve the prognosis. • Pralidoxime –chloride(PAM-Cl)

  32. Characteristic of PAM-CL • The effect of pralidoxime depends on the first time of administration and the dose. The sooner the better.

  33. Characteristic of PAM-CL • It is not effective once the OP compound has bound AChE irreversibly (agedphosphorylated AChE). • For the “aging” time is about 24~36h after poisoning,the pralidoxime should be used within 48h, preferably within 30 minutes.

  34. Characteristic of PAM-CL • T1/2 ＝1-1.5h • Usage: iv. or im. iv gtt.

  35. 2、Anticholinergic drugs—Atropine • Competitively inhibit ACh receptors including receptors found in GI and pulmonary smooth muscle, exocrine glands, heart, and eyes. • In order to relieve the muscarinic symptoms and anti respiratory inhibition.

  36. Atropine • Is a muscarinic antagonist, and thus blocks the action of acetylcholine peripherally • Competitive inhibitor at ACh receptors • No obvious effect on central nicotinic receptors——The effect on convulsion,and respiratory centre depression is poor.

  37. Dosage of anticholinergic drugs • Mild (mg) Moderate(mg) Severe(mg) • Atropine2~4 4~10 10~20 • Administer repeatedly until atropinisation.

  38. Atropinisation • Atropinisationendpoint • Dry axillae; • HR 90-100bpm; • Slight fever,T37.3-37.5℃; • Slight dysphoria; • Pupils no longer pinpoint, facial flushing and chest clear with no rale are reference indexes. • What if you give too much Atropine ? • Anticholinergic Syndrome ： • Delirium,restless,hallucination,convulsion,highfever, Facial flushing,tachycardia,urinary retention. • Sedativesmay help to relieve it.

  39. Proper usage of antidotes • Administer as soon as possible. • Use a combination of a variety of antidotes. • Use adequate dosage for the first time. • Repeated administration according to the patient’s condition.

  40. Comprehensive supportive therapy • 1.Eliminate the source of poisons. • 2.Eliminate the poisons which have been absorbed. • Hemoperfusion • Should be carried out within 24h,and repeated for 1-2 times. • Indication: • Severe poisoning; • Patient’s condition deteriorate with routing therapy; • Liver dysfunction. Charcoal filter

  41. Comprehensive supportive therapy • 3.Keep a patent airway; Inhale O2; Provide adequate oxygenation and ventilation; And administer mechanical ventilation if it is necessary. • 4. Prevent cerebral edema, and use naloxone to ease disturbance ofconsciousness. • 5.Monitor vital sign; Monitor fluid input and output; Treat metabolic disturbances such as electrolyte abnormalities.

  42. The end Thank you! The end Thank you!

More Related